ArticleMolecular and cellular biology1998
Cooperative Pho2-Pho4 interactions at the PHO5 promoter are critical for binding of Pho4 to UASp1 and for efficient transactivation by Pho4 at UASp2.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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43 citing papers in PubMed.
- The nicotinamide mononucleotide adenylyl transferase (NMNAT/Nma1) modulates phosphate-sensing (PHO) signaling independent of its NAD+ synthesis activity in Saccharomyces cerevisiae.FEMS yeast research · 2026Article
- Divergence in a eukaryotic transcription factor's co-TF dependence involves multiple intrinsically disordered regions.Nature communications · 2025Article
- Divergence in a Eukaryotic Transcription Factor's co-TF Dependence Involves Multiple Intrinsically Disordered Regions.bioRxiv : the preprint server for biology · 2025Article
- Identification of Homeobox Transcription Factors in a Dimorphic FungusJournal of fungi (Basel, Switzerland) · 2024Article
- The Histone Deacetylases Hst1 and Rpd3 Integrate De Novo NADInternational journal of molecular sciences · 2023Article
- Nucleosome Remodeling at the YeastInternational journal of molecular sciences · 2023Article
- Systematic analysis of low-affinity transcription factor binding site clusters in vitro and in vivo establishes their functional relevance.Nature communications · 2022Article
- Promoter Architecture and Promoter Engineering inMetabolites · 2020Review
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- Evolution of reduced co-activator dependence led to target expansion of a starvation response pathway.eLife · 2017Article
- The yeast PHO5 promoter: from single locus to systems biology of a paradigm for gene regulation through chromatin.Nucleic acids research · 2014Review
- Mapping the fine structure of a eukaryotic promoter input-output function.Nature genetics · 2013Article
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- The homeobox BcHOX8 gene in Botrytis cinerea regulates vegetative growth and morphology.PloS one · 2012Article
- Integrated approaches reveal determinants of genome-wide binding and function of the transcription factor Pho4.Molecular cell · 2011Article
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- Systematic screen of Schizosaccharomyces pombe deletion collection uncovers parallel evolution of the phosphate signal transduction pathway in yeasts.Eukaryotic cell · 2011Article
- Quantitative analysis of the transcription control mechanism.Molecular systems biology · 2010Article
- Article
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4 authors.
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Abstract
The activation of the PHO5 gene in Saccharomyces cerevisiae in response to phosphate starvation critically depends on two transcriptional activators, the basic helix-loop-helix protein Pho4 and the homeodomain protein Pho2. Pho4 acts through two essential binding sites corresponding to the regulatory elements UASp1 and UASp2. Mutation of either of them results in a 10-fold decrease in promoter activity, and mutation of both sites renders the promoter totally uninducible. The role of Pho4 appears relatively straightforward, but the mechanism of action of Pho2 had remained elusive. By in vitro footprinting, we have recently mapped multiple Pho2 binding sites adjacent to the Pho4 sites, and by mutating them individually or in combination, we now show that each of them contributes to PHO5 promoter activity. Their function is not only to recruit Pho2 to the promoter but to allow cooperative binding of Pho4 together with Pho2. Cooperativity requires DNA binding of Pho2 to its target sites and Pho2-Pho4 interactions. A Pho4 derivative lacking the Pho2 interaction domain is unable to activate the promoter, but testing of UASp1 and UASp2 individually in a minimal CYC1 promoter reveals a striking difference between the two UAS elements. UASp1 is fully inactive, presumably because the Pho4 derivative is not recruited to its binding site. In contrast, UASp2 activates strongly in a Pho2-independent manner. From in vivo footprinting experiments and activity measurements with a promoter variant containing two UASp2 elements, we conclude that at UASp2, Pho2 is mainly required for the ability of Pho4 to transactivate.
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